This phenotype was, surprisingly, rescued by infusion of small amounts of leptin in the third hypothalamic ventricle ( Thomas et al., 1999 Cornish et al., 2002 Takeda et al., 2002). Mice deficient for leptin ( ob/ob mice) were found to have a high vertebral trabecular bone mass phenotype ( Ducy et al., 2000). Investigation into the contribution of neuronal signaling in regulating bone remodeling and homeostasis began with a focus on leptin, an adipose-derived hormone involved in energy regulation and metabolism. The bone remodeling process is regulated by endocrine, paracrine, mechanical, and, as the subject of more recent focus, neuronal factors. However, with age, net bone loss occurs as a result of increased osteoclastic activity and/or decreased osteoblastic activity at a rate of approximately 1% per year after 30 years of age. During this remodeling process, the new bone laid down by osteoblasts must replace the bone resorbed by osteoclasts in a fine-tuned manner. In adult humans, the skeleton replaces itself almost entirely every 10 years. This will encourage a broader view of disease management toward improved patient health and outcomes.Īs an adaptation to stress and to maintain calcium homeostasis, the skeleton undergoes constant remodeling. We also discuss how certain treatments for neurological disorders can negatively affect bone health. This review will provide an overview of literature related to neurological disorders and their effects on bone health with a goal to promote recognition of the mechanisms by which changes in the brain can impart changes in the bones. Likewise, gaining a better understanding of how bones regulate the brain may provide novel insights into how neurological disorders develop. A better understanding of the mechanisms that cause bone loss and how neurological conditions uniquely impact bone health is of clinical importance and will guide treatment options, encourage lifestyle change, and aid in development of novel osteoporosis therapies. Further, lack of physical activity in degenerative neurological conditions can lead to mineral loss and osteoporosis, particularly in aging populations and/or those with comorbidities (e.g., obesity, diabetes, smoking). Osteoporosis is more prevalent in people with neurological conditions, such as multiple sclerosis (MS) and Parkinson’s disease (PD), while sudden neurological events, such as stroke and spinal cord injury (SCI), can cause rapid loss in bone mineral density (BMD). In addition, many of these disorders are associated with increased age, a shared risk factor with osteoporosis. adults are diagnosed annually with a chronic brain disease or disorder at a healthcare cost of > $800 billion ( Gooch et al., 2017). In regard to brain disease, more than one million U.S. By 2050, the costs associated with osteoporotic fractures are expected to exceed $130 billion ( Bartl and Bartl, 2019). In the United States, osteoporosis accounts for over 1.5 million fractures annually. Osteoporosis is the most common form of metabolic bone disease and is characterized by low bone mass (≤ 2.5 standard deviations below peak bone mass) and micro-architectural bone deterioration that can lead to debilitating fractures. One way to better appreciate this relationship is to determine how it becomes altered with disease.
In recent years, we have begun to better dissect the relationship between the brain and skeleton and how they regulate one another. Maintaining bone health is, therefore, important for overall health and well-being. The skeleton is necessary for facilitating movement, providing a framework for muscles and soft tissues, protecting vital organs, storage of minerals and fat, harboring the bone marrow, and regulating blood cell formation.
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